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. 2016 Nov 17;7:13479. doi: 10.1038/ncomms13479

Figure 10. Impaired effects of GW9508 on FGF21-null brown and beige adipocytes.

Figure 10

(a) iBAT precursors from wild-type and FGF21-null mice (n=5) were treated with GW9508 during differentiation, relative transcript levels of UCP1, PGC-1α, Glut1, CoxIV, Sirt3 and FABP4. (b) iBAT precursors from wild-type and FGF21-null mice (n=5) were differentiated and acutely treated with GW9508 (24 h), mRNA expression levels of FGF21, UCP1, PGC-1α, CoxIV, Glut1 and Sirt3. (c) iWAT precursors from wild-type and FGF21-null mice (n=5) were differentiated and acutely treated with GW9508 (24 h), mRNA expression levels of FGF21, UCP1, PGC-1α, CoxIV, Glut1 and Sirt3. (d) Glucose oxidation in iBAT and iWAT-derived adipocytes from wild-type and FGF21-null mice after 24 h treatment with GW9508. Bars are means+s.e.m. (*P<0.05, **P<0.01 and ***P<0.001 for the effects of GW9508; and +P<0.05, ++P<0.01 +++P<0.001 for comparisons between wild-type and FGF21-null cells; and analysis of variance with Tukey's post hoc test). (e) Schematic representation of the effects of GPR120 activation by n-3 PUFAs on brown and beige adipocytes. FGF21 is involved in the GPR120 activation-mediated thermogenic activation of BAT and WAT via autocrine/endocrine mechanisms.